Surgically treated pulmonary inflammatory pseudotumor

We report 2 cases diagnosed as so-called pulmonary inflammatory pseudotumor. In case 1, a 28-year-old man with a slow growing 6-cm pulmonary tumor who underwent a right upper lobectomy was diagnosed with an inflammatory myofibroblastic tumor. In case 2, a 55-year-old man with chest pain and cough, who underwent open lung biopsy was diagnosed with plasma cell granuloma. Despite both diagnoses being classified as pulmonary inflammatory pseudotumors, we believe they should be classified differently.     

Effects of super-pulsed Nd-YAG laser on arterial tissue: comparison with continuous wave

The effects of a super-pulsed Nd-YAG laser at 1.32 μm wavelength on normal or atherosclerotic human arterial tissue were evaluated and compared with those obtained with continuous wave. One joule per pulse was delivered through a 0.2 mm optical fibre with a pulse width of 10 ms at 10 Hz (super-pulse), or 10 W (10 J) were delivered at continuous wave in saline or blood. Ten joules were delivered with super-pulse or continuous wave for each tissue specimen. The aortic specimens were lased either by continuous wave or super-pulse. At super-pulse mode, ablation efficiency (mm³ J⁻¹) was 0.0149±0.0044 for normal tissue in saline, 0.0148±0.0043 for atheroma in saline, 0.0138±0.0062 for normal tissue in blood, and 0.0146±0.0049 for atheroma in blood. There was no significant difference between the groups. At continuous wave mode, ablation efficiency was 0.0507±0.0299 for atheroma in blood (p<0.001 vs super-pulse). However, extensive charring was observed with continuous wave lasing (41% with continuous against 14% with pulsed mode,p<0.001). Heavily calcified plaques were also ablated at 1.5 J per pulse and 15 W (continuous wave), resulting in extensive charring with continuous wave (77% vs 18% with super-pulse,p<0.01). In conclusion, at super-pulse mode, 1.32 μm Nd-YAG laser has neither the selectivity for atheroma nor influence of blood, thermal injury induced by super-pulse is less than that induced by continuous wave (cw), calcified plaques can be ablated by super-pulse, and super-pulsed Nd-YAG laser angioplasty is safer to use than continuous wave.     

Apoptosis of tubular epithelial cells in rats with chronic renal failure

Tubular injury leading to tubular atrophy and tubular loss is one of the characteristic features of chronic renal failure. To reveal the mechanism of tubular atrophy in chronic renal failure, the involvement of apoptosis was studied byin situ nick end labeling of biotinylated deoxyuridine by terminal deoxy nucleotidyl transferase (TUNEL) as well as by electron microscopy. TUNEL-positive cells and heterophagosomes containing apoptotic body-like structures having nuclear fragments with condensed chromatin were observed in the renal tubular epithelium 8 weeks after nephrectomy. It has become apparent from our study that atrophy of the tubules in chronic renal failure results, to some extent, from cell deletion by apoptosis.     

Attenuating effect of castration or oestrogen administration on glomerular injury in adriamycin-induced nephropathy of rats

Summary: To clarify the role of sex-related factors in the development of focal segmental glomerulosclerosis (FSGS) we investigated the effect of castration or oestrogen administration in adriamycin (ADR)-induced nephropathy of Sprague-Dawley rats. At 6 weeks of age, group 1 (control group) and group 3 were shamoperated and group 2 was castrated. Adriamycin 2 mg/kg was administered intravenously to all rats at 8 weeks of age twice at a 20-day interval. Group 3 was administered 0.2 mg oestrogen subcutaneously once a month. Bodyweight (BW) and urinary protein were measured every 4 weeks (mm 15 to 23 weeks of age. Blood pressure and serum constituents were measured at 15 and 23 weeks of age. Each group was studied morphologically at 23 weeks of age. Adriamycin induced massive proteinuria in group 1, whereas castration or oestrogen significantly attenuated proteinuria, accompanied by a significant reduction of urinary sex-related low molecular weight (LMW) protein. the glomerulosclerosis index was significantly higher in the control group than in the castrated group or oestrogen-treated group. Attenuation in glomerular injury was more associated with reduction of urinary sex-related LMW protein than the reduction of serum testosterone. These observations suggest that sex-related factors, such as a sex-related LMW protein, influenced by castration or oestrogen administration may play a contributory role in the development of glomerulosclerosis in ADR-induced nephropathy.     

Effect of ibuprofen on regional eicosanoid production and neuronal injury after forebrain ischemia in rats

Post-ischemic metabolism of arachidonic acid by cyclooxygenase results in the elaboration of numerous eicosanoids and in the generation of free radicals. Accordingly, the effect of cyclooxygenase inhibition by ibuprofen on post-ischemic eicosanoid production and delayed neuronal death was evaluated in Wistar-Kyoto rats subjected to incomplete forebrain ischemia. In control (C) and ibuprofen-treated groups (n = 5 each), pre- and post-ischemic eicosanoid production in the caudate nucleus (CN) and dorsal hippocampus (HPC) were evaluated by microdialysis. The ibuprofen-treated animals were given ibuprofen, 15 mg/kg i.v., prior to insertion of microdialysis probes. Forebrain ischemia was induced by bilateral carotid artery occlusion (BCAO) for 10 min with simultaneous hypotension to 35 Torr. The concentrations of thromboxane B₂ (TxB₂), 6-keto-PGF_1α and PGF_2α in the microdialysate were measured by radioimmunoassay. In two additional concurrent groups of rats (>n = 10 each), neuronal injury in the HPC, CN and cortex (parietal, temporal and entorhinal regions) was evaluated histologically three days after 10 min of forebrain ischemia with and without pre-ischemic ibuprofen administration. In the control microdialysis group, levels of TxB₂, 6-keto-PGF_1α and PGF_2α increased in both CN and HPC after probe insertion. These probe related increases were substantially reduced in the ibuprofen group. After ischemia and reperfusion in the control group, the levels of TxB₂ and PGF_2α increased in both CN and HPC. Levels of 6-keto-PGF_1α increased in the CN but not in the HPC. The administration of ibuprofen substantially reduced post-ischemic TxB₂ and PGF_2α levels in both CN and HPC and decreased 6-keto-PGF_1α levels in the CN. The results of these initial microdialysis studies left the possibility that, in the ibuprofen group, the reduction in eicosanoid levels after probe penetration might have influenced the subsequent post-ischemic eicosanoid production. Therefore, in an additional group of animals (n = 5), ibuprofen was administered after probe insertion. Only PGF_2α levels were measured in this group. Increased levels of PGF_2α comparable to the original control group were detected after probe penetration. Nonetheless, after ibuprofen administration, the pre- and post-ischemic levels of PGF_2α were again significantly reduced. In the histologic evaluation groups, overall neuronal injury was significantly less in the ibuprofen treated animals. This protective effect of ibuprofen was most clearly evident in the CA3 sector of the HPC. The data suggest that metabolism of arachidonic acid by cylooxygenase may contribute to post-ischemic neuronal injury, though the relative contributions of eicosanoids per se and of free radicals remains undefined.     

The impact of hepatitis C virus infection on liver disease in renal transplant recipients

Abstract To assess the prevalence of hepatitis C virus (HCV) infection in renal transplant recipients and its impact on posttransplant liver disease, the sera from 176 recipients who had been followed for 1–20 years (mean 8.3 years) were tested for HCV-pecific antibody using enzyme immunoassay. HCV-pecific antibody was detected in 53 patients (30.1%) including 2 patients also positive for hepatitis B surface antigen (HBsAg). Among 167 HBsAg-negative patients, the presence of HCV-pecific antibody was associated with an increased incidence of chemically significant hepatitis (70.6% vs. 9.5% in anti-HCV-negative patients, P<0.01). Hepatitis was more likely to be chronic in anti-HCV-positive patients than in anti-HCV-negative patients (P<0.05) Serious liver disease developed in 4 of 51 anti-HCV-positive, HBsAg-negative patients: liver failure causing death in 3 and hepatoma in 1. Liver biopsy specimens from anti-HCV-positive patients showed more aggressive histological lesions compared with those from anti-HCV-negative patients. We conclude that HCV infection is quite prevalent in our renal transplant recipients and plays a major role in posttransplant chronic liver disease.     

Two cases of radiofrequency ablation (RFA) therapy for control of liver metastases from breast cancer

We present two cases of liver metastases from breast cancer treated by radiofrequency ablation (RFA) for elongation of life. Case 1: A 50-year-old woman was treated by left mastectomy (stage IIIa) in December 2002. In April 2004, she was treated with a combination therapy of weekly paclitaxel and trastuzumab for multiple liver metastases, left supraclavicular lymph node metastases, and multiple bone metastases. After 16 courses of weekly paclitaxel and trastuzumab, liver metastases decreased significantly in size. Because liver metastases recurred during a continuation of weekly paclitaxel and trastuzumab, we performed RFA and chemotherapy using a hepatic artery infusion of docetaxel for liver metastasis. The aggravation spread to the liver lesion and she died after 20 months from liver metastases. Case 2: A 65-year-old woman was treated by left mastectomy (stage IIA) in 1984, and the distant metastasis was not found through the course after an operation. She was noted with a liver function aberration in another hospital in March 2005. We scanned it, and it was diagnosed as multiple liver and bone metastases from breast cancer. Because she did not hope for an anticancer drug treatment for multiple liver metastases, we performed RFA in May 2005. After the second RFA was performed, she does not show any new lesion to the liver for 10 months.     

Esophageal squamous cell carcinomas with distinct invasive depth show different gene expression profiles associated with lymph node metastasis

We examined the gene expression profiles of esophageal squamous cell carcinomas (ESCCs) with respect to degree of invasive depth and lymph node (LN) involvement in a large cohort. We used high-density oligonucleotide microarrays to examine the expression of 22,115 genes in 54 ESCCs and 11 non-cancerous esophageal tissues. We found that 4,155 genes were biologically significant in both ESCC and non-cancerous esophageal tissue by analysis of Present Call (hybridization quality by Affymetrix) throughout all samples. From these genes, we used a supervised learning method to select genes responsible for the development of ESCC. We found that 999 genes were expressed differentially in pT1/pN0 tumors vs. non-cancerous esophageal tissue. In the same manner, 48, 66 and 30 genes were expressed differentially in pT1/pN0 tumors vs. pT1/pN1 tumors, pT1/pN0 tumors vs. pT2-4/pN0 tumors and pT2-4/pN0 tumors vs. pT2-4/pN1 tumors, respectively. Intriguingly, there were no overlaps between the 48 LN metastasis-related genes of pT1 tumors and the 30 LN metastasis-related genes of pT2-4 tumors, suggesting that ESCCs with distinct invasive depths express different genes linked to LN metastasis. Our present results suggest that the degree of invasive depth must be considered when predicting LN metastasis of ESCC from gene expression profiles.